Mentions:
Mitochondrial Parameters. There were similar levels of Sirt1 in the striatum and hippocampus. As shown in Figures 2(a) and 2(b), a decrease in Sirt1 was observed in the U + 6-OHDA group compared with the Sham group. However, only treadmill training attenuated this decrease in the striatum. Both treadmill training and strength training attenuated the decrease in Sirt1 in the hippocampus. There was a significant decrease in complex I activity in the U + 6-OHDA group compared with the Sham group (Figures 2(c) and 2(d)). However, both striatal and hippocampal complex I levels increased significantly in the STR + 6-OHDA and TTR + 6-OHDA groups compared with the U + 6-OHDA group.

Mentions:
Mitochondrial Parameters. There were similar levels of Sirt1 in the striatum and hippocampus. As shown in Figures 2(a) and 2(b), a decrease in Sirt1 was observed in the U + 6-OHDA group compared with the Sham group. However, only treadmill training attenuated this decrease in the striatum. Both treadmill training and strength training attenuated the decrease in Sirt1 in the hippocampus. There was a significant decrease in complex I activity in the U + 6-OHDA group compared with the Sham group (Figures 2(c) and 2(d)). However, both striatal and hippocampal complex I levels increased significantly in the STR + 6-OHDA and TTR + 6-OHDA groups compared with the U + 6-OHDA group.

Bottom Line:
Strength training increased CI activity and TH and Sirt1 levels and reduced NO, NF-κB p65, TNF-α, IFN-γ, IL-1β, and TGF-β1 levels in 6-OHDA mice, while treadmill exercise increased CI activity and NO, TH, and Sirt1 levels and reduced NF-κB p65, TNF-α, IFN-γ, and IL-1β levels.Our results demonstrated that both treadmill training and strength training promote neuroprotection, possibly by stimulating Sirt1 activity, which may in turn regulate both mitochondrial function and neuroinflammation via deacetylation of NF-κB p65.Changes in nitric oxide levels may also be a mechanism by which 6-OHDA-induced inflammation is controlled.